Apc inhibition of Wnt signaling regulates supernumerary tooth formation during embryogenesis and throughout adulthood

AUTOR(ES)

Wang, Xiu-Ping

FONTE

Company of Biologists

RESUMO

The ablation of Apc function or the constitutive activation of β-catenin in embryonic mouse oral epithelium results in supernumerary tooth formation, but the underlying mechanisms and whether adult tissues retain this potential are unknown. Here we show that supernumerary teeth can form from multiple regions of the jaw and that they are properly mineralized, vascularized, innervated and can start to form roots. Even adult dental tissues can form new teeth in response to either epithelial Apc loss-of-function or β-catenin activation, and the effect of Apc deficiency is mediated by β-catenin. The formation of supernumerary teeth via Apc loss-of-function is non-cell-autonomous. A small number of Apc-deficient cells is sufficient to induce surrounding wild-type epithelial and mesenchymal cells to participate in the formation of new teeth. Strikingly, Msx1, which is necessary for endogenous tooth development, is dispensable for supernumerary tooth formation. In addition, we identify Fgf8, a known tooth initiation marker, as a direct target of Wnt/β-catenin signaling. These studies identify key mechanistic features responsible for supernumerary tooth formation.

Documentos Relacionados

• Wnt/Shh interactions regulate ectodermal boundary formation during mammalian tooth development
• Wnt-1 regulates free pools of catenins and stabilizes APC-catenin complexes.
• Noncanonical Wnt signaling regulates midline convergence of organ primordia during zebrafish development
• Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration
• Ecsit is required for Bmp signaling and mesoderm formation during mouse embryogenesis